Kumar K, Krause G, Koestner A, Hoehner T, White B
Exp Neurol. 1987 Jul;97(1):115-27. doi: 10.1016/0014-4886(87)90286-x.
The effects of flunarizine, a calcium antagonist, were evaluated in an experimental model of global brain ischemia produced by 15 min of cardiac arrest followed by resuscitation and reperfusion. One group of dogs received flunarizine (0.1 mg/kg intravenously during a 10-min period) at the onset of resuscitation. Another group of dogs underwent cardiac arrest, resuscitation, and reperfusion but did not receive flunarizine. A third group served as nonischemic control. In situ-fixed brains of all animals (nonischemic controls and the postischemic dogs after 8 h of reperfusion) were examined for anoxic ischemic injury. Quantitation of the ischemic neurons was carried out in parietal cortex, hippocampus, and cerebellum by using an image analysis system. Significant difference in the number of necrotic neurons between the flunarizine-treated group and the ischemic controls was noted in the hippocampus only; the mean percentage of necrotic neurons in the two groups being 14.8 +/- 9.6 and 29.3 +/- 12.1, respectively (P less than 0.05). These results indicate that flunarizine has an ameliorating effect on neuronal injury in the hippocampus that follows cardiac arrest in this experimental model of global brain ischemia. However, flunarizine was not found to be effective in reducing the ischemic neuronal damage in the cortex or the cerebellum.
